A hallmark condition of bronchial asthma is an increased sensitivity to the deleterious effects of histamine. A similar increase in histamine sensitivity has been observed in Bordetella pertussis vaccinated mice. The mechanism by which histamine hypersensitivity arises in either case is currently unknown. It does not, however, involve either increased synthesis, decreased degradation or increased retention of histamine by the body. It has been suggested that this histamine hypersensitivity may involve alteration in the functional state of the enzyme adenylyl cyclase resulting in abnormal catecholamine action or possibly altered vascular permeability. Recently it was observed that pertussis vaccinated mice challenged with histamine responded with an increased accumulation of what appears to be cyclic 3',5'-adenosine monophosphoric acid (cyclic AMP) in their lung tissue. Verification and evaluation of the possible causal role between this increased accumulation of cyclic AMP and histamine death may reveal the biochemical nature of the pertussis induced histamine hypersensitivity, which may parallel that observed in human asthma. If so, this model might be useful to (1) further define biochemical changes in asthma, and (2) screen potentially useful therapeutic agents.